Esipova V V, Zavil'gel'skiĭ G B, Kriviskiĭ A S
Genetika. 1977;13(10):1801-8.
The sensitized irradiation (lambda greater than 310 nm) with AcphiM induces plaque mutants of extracellular phage Sd. Thus, TT in phage Sd DNA are both lethal and mutagenic. The yield of plaque mutants is about 3-fold lower as compared with the yield after UV-irradiation (lambda = 254 nm). The theoretical analysis of UV-induced mutagenesis curves of phage Sd was carried out. It is concluded that the following photoproducts make a contribution in the mutagenic effect of near-UV (lambda = 254 nm): 1) lethal pyrimidine dimers; 2) other lethal photolesions; and 3) non-lethal mutagenic photoproducts of cytosine. The cytosine photohydrate contribution nearly twice exceeds the total contribution of lethal photoproducts. It is assumed that bacteriophages T4 and Sd have their own system of repair, like SOS-repair in bacteria.
用AcphiM进行敏化照射(波长大于310nm)可诱导细胞外噬菌体Sd的噬菌斑突变体。因此,噬菌体Sd DNA中的胸腺嘧啶二聚体既是致死性的又是致突变性的。与紫外线照射(波长=254nm)后的产量相比,噬菌斑突变体的产量约低3倍。对噬菌体Sd的紫外线诱导诱变曲线进行了理论分析。得出以下结论:以下光产物对近紫外线(波长=254nm)的诱变作用有贡献:1)致死性嘧啶二聚体;2)其他致死性光损伤;3)胞嘧啶的非致死性诱变光产物。胞嘧啶光水合物的贡献几乎比致死性光产物的总贡献高出两倍。假定噬菌体T4和Sd具有自身的修复系统,类似于细菌中的SOS修复。